VISCOELASTIC RELAXATION AND REGIONAL BLOOD-FLOW RESPONSE TO SPINAL-CORD COMPRESSION AND DECOMPRESSION

Study Design. To better understand the relationships between primary m echanical factors of spinal cord trauma and secondary mechanisms of in jury, this study evaluated regional blood flow and somatosensory evoke d potential function in an in vivo canine model with controlled veloci ty spinal cord displacement and real-time piston-spinal cord interface pressure feedback. Objectives. To determine the effect of regional sp inal cord blood flow and viscoelastic cord relaxation on recovery of n eural conduction, with and without spinal cord decompression. Summary of Background Data. The relative contribution of mechanical and Vascul ar factors on spinal cord injury remains undefined. Methods. Twelve be agles were anesthetized and underwent T13 laminectomy. A constant velo city spinal cord compression was applied using a hydraulic loading pis ton with a subminiature pressure transducer rigidly attached to the sp inal column. Spinal cord displacement was stopped when somatosensory e voked potential amplitudes decreased by 50% (maximum compression). Six animals were decompressed 5 minutes after maximum compression and wer e compared with six animals who had spinal cord displacement maintaine d for 3 hours and were not decompressed, Regional spinal cord blood fl ow was measured with a fluorescent microsphere technique. Results. At maximum compression, regional spinal cord brood flow at the injury sit e fell from 19.0 +/- 1.3 mL/100 g/min to 12.6 +/- 1.0 mL/100 g/min, wh ereas piston-spinal cord interface pressure was 30.5 +/- 1.8 kPa, and cord displacement measured 2.1 +/- 0.1 mm (mean +/- SE), Five minutes after the piston translation was stopped, the spinal cord interface pr essure had dissipated 51%, whereas the somatosensory evoked potential amplitudes continued to decrease to 16% of baseline. In the sustained compression group, cord interface pressure relaxed to 13% of maximum w ithin 90 minutes; however, no recovery of somatosensory evoked potenti al function occurred, and regional spinal cord blood flow remained sig nificantly lower than baseline at 30 and 180 minutes after maximum com pression. in the six animals that underwent spinal cord decompression, somatosensory evoked potential function and regional spinal cord bloo d flow recovered to baseline 30 minutes after maximum compression. Con clusions. Despite rapid cord relaxation of more than 50% within 5 minu tes after maximum compression, somatosensory evoked potential conducti on recovered only with early decompression. Spinal cord decompression was associated with an early recovery of regional spinel cord blood fl ow and somatosensory evoked potential recovery. By 3 hours, spinal cor d blood flow was similar in both the compressed and decompressed group s, despite that somatosensory evoked potential recovery occurred only in the decompressed group.